Figure 2

Figure 2

Cadmium toxicity is dependent on functional mechanotransduction activity. (A)cdh23^tj264 mutants, which lack functional mechanotransduction activity, are resistant to cadmium-induced hair cell death. (B) Representative images of the O2 Neuromast in wild-type siblings (top) and cdh23 mutants (bottom) fish following treatment with either 0 (left) or 60 (right) μM cadmium chloride. (C) Treatment with 200 μM Benzamil, a mechanotransduction channel blocker, significantly blocks cadmium-induced hair cell death as compared to fish treated with the same amount of DMSO alone (a 1:200 dilution). (D) Representative images of the O2 Neuromast in DMSO-treated (top) and benzamil treated (bottom) fish following treatment with either 0 (left) or 60 (right) μM cadmium chloride. Due to reduced hair cell numbers in cdh23 mutants data is normalized to the 0 cadmium chloride control for each treatment group. Data are displayed as mean ± standard deviation. *p < 0.05, ****p < 0.0001 by Two-Way ANOVA and Šídák multiple comparisons test. Black stars above the error bars denote significant differences in cdh23 mutants or benzamil treated fish as compared to their respective wild-type sibling and DMSO control groups treated with the same dose of cadmium chloride. Gray stars below the error bars denote significant differences in cdh23 mutants or benzamil treated fish at that cadmium chloride dose compared to the 0 cadmium chloride control group of the same mutant or drug condition. n = 10 fish for all groups.